These projects are steps in the overall goal of utilizing intracellular indicators of oxidative metabolic activity to assess changes that occur during cerebral ischemia and to determine the factors most critical to overall tissue viability during and following periods of circulatory compromise. Non-invasive techniques of fluorometrically monitoring reduction/oxidation changes of NAD and reflection spectrophotometry to measure redox changes of cytochromes will be utilized. The advantage of these procedures is that they require no invasive assay sampling and allow the tissue to remain intact, normally or abnormally circulated with normal cellular, anatomical and physiological relationships intact. Simultaneous to detection by these metabolic techniques, parameters of electrophysiological function such as steady potn-tials, ECoG, evoked potentials and perhaps the level of extracellular potassium will be recorded from the same tissue area. By relating parameters of metabolism and function, we may discern how vulnerability of function activity of the cerebral cortex is associated with periods of ischemic insult. We will continue efforts to establish relationships between energy metabolism and cortical functioning to increase our understanding of how and why the brain utilizes oxygen, metabolic substrates and oxidative energy and to determine how viability is threatened by the loss of oxygen and circulatory perfusion.